HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 292/3/H1435    most recent 00282.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Yamaguchi, T. Articles by Korthuis, R. J. Search for Related Content PubMed PubMed Citation Articles by Yamaguchi, T. Articles by Korthuis, R. J.

Role of eNOS-derived NO in the postischemic anti-inflammatory effects of antecedent ethanol ingestion in murine small intestine

¹Department of Medical Pharmacology and Physiology and the Dalton Cardiovascular Research Center, University of Missouri-Columbia School of Medicine, Columbia, Missouri; ²Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, School of Medicine, Shreveport, Louisiana; and ³First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan

Submitted 17 March 2006 ; accepted in final form 6 November 2006

Ingestion of low levels of ethanol 24 h before [ethanol preconditioning (EPC)] ischemia and reperfusion (I/R) prevents postischemic leukocyte rolling (LR) and adhesion (LA), effects that were abolished by adenosine A₂ receptor (ADO-A₂R) antagonists or nitric oxide (NO) synthase (NOS) inhibitors. The aims of this study were to determine whether NO derived from endothelial NOS (eNOS) during the period of ethanol exposure triggered entrance into this preconditioned state and whether these events were initiated by an ADO-A₂R-dependent mechanism. Ethanol or distilled water vehicle was administered to C57BL/6J [wild type (WT)] or eNOS-deficient (eNOS–/–) mice by gavage. Twenty-four hours later, the superior mesenteric artery was occluded for 45 min. LR and LA were quantified by intravital microscopy after 30 and 60 min of reperfusion. I/R increased LR and LA in WT mice, effects that were abolished by EPC or NO donor preconditioning (NO-PC). NO-PC was not attenuated by coincident administration of an ADO-A₂R antagonist. I/R increased LR and LA in eNOS–/– mice to levels comparable with those noted in WT animals. However, EPC only slightly attenuated postischemic LR and LA, whereas NO-PC remained effective as a preconditioning stimulus in eNOS–/– mice. Preconditioning with an ADO-A₂R agonist (which we previously demonstrated prevents I/R-induced LR and LA in WT animals) failed to attenuate these postischemic adhesive responses in eNOS–/– mice. Our results indicate that EPC is triggered by NO formed secondary to ADO-A₂R-dependent eNOS activation during the period of ethanol exposure 24 h before I/R.

ischemia; reperfusion; adenosine; nitric oxide; leukocyte rolling; endothelial nitric oxide synthase knockout mice

This article has been cited by other articles:

				M. Yusof, K. Kamada, T. Kalogeris, F. S. Gaskin, and R. J. Korthuis Hydrogen sulfide triggers late-phase preconditioning in postischemic small intestine by an NO- and p38 MAPK-dependent mechanism Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H868 - H876. [Abstract] [Full Text] [PDF]